Review Article

Metal Toxicity at the Synapse: Presynaptic, Postsynaptic, and Long-Term Effects

Table 3

Effects of metals on transporters, neurotransmitters, and neuropeptides (↑—activation/upregulation, —inhibition/downregulation).

TargetTransportersNeurotransmittersNeuropeptides
Ca2+ into mitochondriaCa2+ ATPaseDopamine transporterGlutamateAspartateGABAGlycineDopamineAcetylcholineSubstance P, neuropeptide K, and neurokinin

AlEffect
Conc0–100 μM
Ref[2]

CdEffect( v )( v )(v)(v)
Conc10–30 μM10–30 μM10–30 μM10–30 μM5(iii)μM
Ref[31][31][31][31][32]

CuEffect
Conc10(i)μg m−1
Ref[33]

HgEffectNCh
Conc400 μM6 mg/kg, 400 μM
Ref[34][35], [34]

MnEffect
Conc20–200 nm(iv)20–200 nm20–200 nm10(ii)μg mL−1
Ref[36][36][36][33]

NiEffect
Conc
Ref[37]

PbEffect
Conc50 μmol L−1100 μmol L−1
Ref[38][39], [38][39]

PtEffectNC
Conc0.5 mM500  μM
Ref[40][41]

SnEffect
Conc10–100 μM
Ref[42]

(i)Upregulates expression of monoamine oxidase, decreases production, and increases depletion
(ii)Downregulates expression of tyrosine hydroxylase gene
(iii)Reduces expression of precursor gene
(iv)Another study shows that uptake of glutamate into astrocytes is reduced through the decreased expression of glutamate aspartate transporter; this may result in increase in glutamate levels in the synapse [43]
(v)Shows effect on neurotransmitter release.